An obesity syndrome has been observed in mice infected intracerebrally with herpes simplex viruses (HSV) typs 1 and 2. To moderate or overcome the pathogenic effect of the viruses, potent selective antivirals were used; thus a larger number of mice survived the primary infection. At 8 weeks post-infection, about 6% of 476 surviving 14 - 16 week-old mice became jobese, whereas none of the 107 phosphate-buffered saline-inoculated mice developed obesity. The proposed studies will be undertaken to evaluate the incidence of obesity in mice as function of age when infected (weanling, 7 weeks, 3 months and 6 months old Swiss outbred female mice). The age of infection is important since virus may interfere (directly or indirectly) in the development of adipocytes at various stages of the growth of the mice. Several parameters of adipose tissue cellularity will be examined. Preliminary metabolic studies will be carried out including measurements of food intake, thyroid metabolism and serum cholesterol levels. Once this model is well developed, other parameters such as size and route of virus inocula, virulence of the virus, genetics of the virus and the host and condition of the host could be explored. It is well established that obesity accelerates aging and our mouse obesity model indicates that viruses such as HSV can cause obesity. This proposal will examine prospectively the effect of age at which virus intervention occurs on the incidence and degree of obesity in mice, in order to build a better model for the interaction of viruses on the aging process in this new model for the study of obesity.